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Adenotonsillar hypertrophy as a cause of failure to thrive

ANN CS! ll+l lt\N, MR, MRCPI, R BRENT Sc '.t)TT, MDCM, FRCPC, I !ELIN M MA< 1 IIDA, MD, FRCPC

ABSTRACT: Two infant aged 11 anJ 15 mo nths presented to the Gastro­t'ntemlngy C linic at Alberta Children's Hospital hecause of failure to thrive. Clinical ,m~ lriboratory investigations excluded any underlying abnormali1y of 1he gastrointest inal tract. Because of a history of obstructive upper respiratory ~\'mptoms, both were referred for ear, nose and throat evaluation, and both were found to have partial upper airway obstruction secondary lo adenotons11lar hypertrophy. Subsequent a<lcnotonsillectomy led to resolution of obstructive upper rc,p1ratory symptoms and dramatic increases in weight gain and growth. Adenmons11lar hypertrophy should he mcluded among the potential causes of t.ulurc to thrive 111 infancy, especially if the child has a history of obstruc tive upper respiratory symptoms. Can J Gastroenterol l 990;4(8):485-488

Key Words: Adenotonsillar hypertrophy, Failure to chrrve

Hypertrophic adeno,amygdalienne et retard de croissance

RESUME: Dcux jcunes enfants ages Je 11 Cl 15 mois Ont cte conduits a la clm1quc de gastro-cntcrologie de !'Alberta C hildren\ Hospital pour retard Je m11ssance. Les examens cliniqucs ct Jc laboratoire n'ont revclc aucune anomalic ,ous-jaccnte des voics gastro-intestinales. Ayant auparavanc presente des trnuhb ohstructifs des voies afriennes superieures, tous Jcux ont ete envoyes e n ORL pour suhir unc evaluation. Elle a revcle une obstruction particlle des voics .1rnenncs superieures secondaire a une hypertrophie adcno-amygdalicnne. Une ,1Jcno- amygdalecro mie a conduit a la resolutio n Jes symptomes ct resultc en une augmentation spectaculaire du poids ct de la ta1lle des patients. L'hypertrophie aJeno-amygdaliennc dcvrait figurer parmi lcs causes possibles de retard de ,ro1ssance chez les nourris ons, surtout chez l'enfant qui presence Jes troubles 0hmuctifs des voies aericnnes superieures.

:\l~rtaChildren's I losfmal, Unrl'l'rmy ofC<1lgaT)'. Calgary, /\ll>ena Cmmprmdence and re/mnts: Dr/ le/en Maduda, All>erra Children's I Im/ma/. / 820

Rrchmond Road S\'v', Calgan. Alhena T2T 5C7 T elephon<' ( 403) 229 72 11 Receit-ecl far puhlicaucm April 25, 1990. Acc<'/H<'cl J lll'I 24, / 990

TONSILLH'TOMY AND ADFNOl[)F('

tomy rc1m11n the most common maior operations c.imed tlUl in child­lwod ( I ). Surgical md1cat1111v, vary from recurren t or chronic tons1 l1 1t1s and otitis media to rhe more extreme alvl'· nlnr hypovenulation wnh cm rulmn­nale ( l ). Recently, 11 was rccngnizcd that adcnotonsillar hypenwphy may abo present as failure co thrive wh ich resol ­ves wi t h tons ill ecwmy and aden­rndcctrnn~ (2-9). Two similar cases arc rcpt)rted m which children riged 11 and 15 months, respectively presented with fa ilure to thrive due 1n parual upper airway ohstruct io n from tonsdlar and adenoida l hypertrophy. In hmh chil­dren, tonsillectomy and adcnrndccto­my resul ted in dramatic weight gain and catch-up growl h. These rnses arc re­ported to increase awareness of this re­cently recognized clinKal entity, ,mJ ro emphaMze the importance of an ear, nose and throat evaluation in an infant who presents with horh failure ro rhnve and ohstructivc upper resp1rnrory symptoms.

CASE ONE An 11-monrh-old female was re­

fer red co the tH1tpat1ent (,astrn­entemlogy Clinic at Alhena Children's

48'i

s, IEEHAN et al

GIRLS: BIRTH TO 36 MONTHS PHYSICAL GROWTH NCHS PERCENTILES

BOYS: BIRTH TO 36 MONTHS PHYSICAL GROWTH NCHS PERCENTILES

42

15

14

12

1()

9 8 7 6 5

3 1 301 29 28' 27 ?6 2~

19 18 17 16 15 14

13 12

Figure 1) \~ eight and height before and after adenownsill.eccomy in case ( left) and case 2 ( right) illustrating the weight gain which followed adenoronsillecwm'I

H ospita l. U niversity of Calgary, be­cause of fai lure to thrive.

She haJ been the product of a nor­mal pregnancy with a birth weight of 341 0 g (75th percentile). She was breastfed from birth. Pablum and cere­a ls were introduced at five months, with progression to pureed cable food shortly thereafter. Who le milk was started at nine months. The patient's history was unremarkable apart from very frequent upper respiratory tract infections: eight in the previous six months. There was also a history of laboured mouth breath­ing and markeJ snoring during sleep. Detailed dietary history revealed a caloric intake equa l to 66% of recom­mended dietary allowances. The fall-off in the patient's height and weight is illustrated in Figure I.

486

The patient's parents, her 10-year­old brother and four-year-old sister were wel l. The younger sibling had had a fund oplication for gasrroesophageal reflux. A paternal cousin had three children wi th cystic fibrosis.

Phys ical examinatio n revealed a thin wasted infant whose weight of 5.82 kg was below the fifth percentile, and whose he ight of 69 cm was greate r than the 25th percenti le. S he had nasal con­gest ion and rhino rrhea, and was mouth breathing. Her tonsils were enlarged but nor inflamed and met in the mid­line. Examination was otherwise un­remarkable.

Laboratory investiga tions including complete blood count, prothrombin time, partia l thromboplast in tim e, calcium, phosphorus, alkaline phospha-

case, total protein, a lbumin, clecmi­lytes, urea , creatinine, liver function tests, serum immunoglobulins, chole­sterol, urine metabo lic screen including amino ac ids and organic acids, thy­roxine and thyroid stimulating hor­mone levels were a ll normal. Urinalysis and cul ture were negative. A three-day quantitat ive feca l fat collect ion was normal with an excretion of 3% of in­take. The sweat chloride was normal at 7 mmol/L.

Two subsequent outpatient visits revealed pe rsiste nt anorexia with failu re to ga in weight. Because of chronic post nasa l airway obstruction, lo ud snoring a t nigh t and mouth breathing, an ear, nose and throat con­s ult was req ues ted. Ex aminat ion revealed no serviceable nasal airway

CAN J GASTROENTEROL VOL 4 No 8 N OVEMBER/DECEMBER 1990

due to enlarged adenoids a n<l oral ex­amination again demonstrated grossly enlarged but no ninflame <l tonsib couching at the mic.lline. As it was thought that severe adenotonsi llar hy­pertrophy was contributing significant ­ly to the infant's anorexia and poor weight ga in , ton s illeCLo my and adenoi<leccomy were performe<l at the age of one year.

One week priorto surgery, the infant was admitted for supplementa l night­time nasogastric feedings to improve nutritional status. These feeds were dis­continued postoperatively as oral in­take impro ved. Two mo nth~ afte r adenoronsillectomy she had gained 1. 2 kg. At 19 months, her weight was 9. 5 kg {10th percentile), and her height was 710 cm (25th percentile ). Her we ight as a pe rcentage of ideal we ight for height before surgery was 72.5% and after surgery at 19 momhs it was 96%.

CASE TWO A I 5-month-ol<l male was referred

to the outpatient Gastroe nterology Clinic because of failure to thrive.

History revealed a normal delive ry at term wit11 a birth weight of 3380 g. He was breastfed for seven weeks a nd then switch ed to S imilac (R oss La b­oratories). At three and four months of age, he had acute gastroenteritis and dehydration requiring hospita lization. After the second admission, he was switch ed LO Nutramigen (M ead Johnson). In addition, for the first seven months of his life, the patient had upper respiratory infections with a ch ronic cough, nasal congestion and rh inor­rhea. During this time he was given at least iO courses of an tibiotics.

At eight mo nths he was started on whole cow's milk. From eight co 29 months, inte rval examinatio n s revealed a thin wasted child whose weight was consistently below the fifth percentile and whose height was be­tween the 25th and 50th percentiles (Figure l ). He was a mouth breather with nasal speech and his consils were enlarged but not inflamed . At 20 months, asthma was diagnosed and he was started on theophylline (Somo­phytlin; Fisons) and salbutamo l (Ven­tolin; Glaxo).

Both parents we re welt, buL his mother had been on a gluten-free JieL since infancy because of a clinical d iag­nosis (not biopsy prove n) of celiac dis­ease. A two-an<l -a-half-year-old sibling was healthy.

S ubsequent laboratory investiga­tions inclu<ling a complete blood count, prothrombin time, partial rh romboplas­tin time, calcium , phosphorus, alkaline phosphatase, total protein, a lbumin , elec trolytes, urea , creatininc, urine me­tabolic screen including amin1) and or­ganic ac ids, live r funct ion tesLs and c ho lestero l were normal. A three-Jay quantitati ve fecal fat collection showed an excretion of 0.8% of intake, anJ a ca lo ric intake that met the recom­mended daily allowance for age. A je­juna! biopsy showed norma l vil lo us architecture. SweaL c hlo ride was 9 mmot/L.

At 29 momhs the child continued to have intermittent upper respiratory in­fections. A blocked nasal airway an<l c hronic mouth breathing made eating difficult. At night he snored loudly and awakened imermittently with resp­iratory diffic ulty Jue to partia l upper airway obstructio n wh ic h was not asthma. His weight of 10 kg remained al less than the fifth percentile. O n exa mination, he ha J a complete ly obstructed upper a irway a nd was drool­ing because of constant mouth breath­ing. Post n asa l space x- ray showed adenoida l hypertrophy and posterior tons illar enlargement. Maxillary s inuses were opaque. A ronsillecwmy and adenoidectomy were performed.

O n e mo nch laLe r the child was eating well, breathing through his nose and sleeping throughout the night. He had gained 1.6 kg. Three months later and still well, his we ight ha<l increased to 12.2 kg (between the fifth and 10th percentiles) and his he igh t of90cm was on the fifth to 10th pe rcentile. His weight as a percentage of ideal weight for height before surgery was 89% and two mo nths postope rative ly it was 100%.

Seven months poscoperatively, he was again symptoma tic with anorexia, inc reased mouth breathing a nd snoring. His weight of 15.5 kg remained in the 10th to 25th percentile. S inus x-rays

CAN J GASTROENTEROL VOL 4 N o 8 N OVEMBER/DECEMBER 1990

Adenotonsillor hypertrophy

and high kilovo lLage views of Lhe neck showed e nlargement of the re~idual adenoidal tissue and hi lateral opacifica­rion of the maxillary sinuses. Ear, nose and throat exa minati o n revea led prominent inferior turbinates obstruct­in g the nasal airway. A repeat adc noidectomy was performed with submucosal diathermy of inferior tur­binates. The p,1tient d iJ wcl I postopera­Li ve l y and had n ormal subsequent growth ve lociLy.

DISCUSSION Among Lhe more commonly en­

counr ered prohle ms seen in ,1 pediatric gastroenterology clinic is thaL of the infant or child who is fa iling to thrive. The d ifferential diagnosis includes v ir­LUally every chronic disease of c hild­hood. Fortunately, a probable diagnosis can generally he reached hy a thorough history and physical cxaminaLion (1 0).

There was a delay in diagnosis in both of these cases (only one month in the firsL case, but a lmost I 4 months in the second) . The delay is partly amibu­rable to the fact that fi ve LO e ight upper respi ratory tract infecLions per year are within normal limits for Lhis age group and can result in temporary adenoton­sillar hypertrophy. In retrospect, in case 2, Lhe significant contribution of per­sistent respiratory symptoms to the fa il ­ure to thrive was not appreciated. As a result , exLensive invest igat ions were carried o ut which did not idemify the unde rlying prohlem. Ir is only in recent years that adenotonsillar hypertrophy causing obs tructive s leep apnea has been recognized as a cause of growth fai lure, which can be Lreated with re­moval of tonsils and adenoids (2-9 ). Previous reports have a lso highlighted this delay in diagnosis (9). Brouillette e t a l (9) felt that there were two possible contributing factors: first, a lack of awa reness of the entity, and second, the fact that most chi ldren look surprisingly normal when awake, despite snoring re­tractions and inte rmittent complete obstruction when asleep. Delay in d iag­nosis may have serious consequences, as ch ronic proble ms can result in fail ure to

thrive, <levelopmental delay and cor pulmona le (9-12).

O bst ruc t ive sleep apnea was de-

487

SHEEI IAN et al

scribed in adults in 1966. However, the entity was first reported in children by Guilleminault in 1976 ( 11 ). The most common cause of this type of partial upper a irway obstruction in children was adenotonsillar hypertrophy. A vari­ety of symptoms and signs are described. During the day, there is often excessive s leep iness, mouth breathing, beh a­vioura l changes an<l respiratory conges­tion. A more recent report suggests that vomiting may be a feature of obstructive sleep apnea (3 ). However, most fre­quently, symptoms occur at night and include excessive snoring, restless sleep, arousal during sleep, and apnea ob­served by the parents. Confirmation of the diagnosis can be Jone by observing patients during sleep, and by poly­graphic recordings that demonstrate hypoxernia (Pa02 less than 50 mmHg), hypercarbia (PaCOz more than 45 mmHg) and changes in heart and re­spiratory rate consistent with obstruc­tive apnea. In Brouillette's review (9), the mean age of onset of symptoms was 21 months, bur there are reports of in­fants requiring adenotonsi lleccomy as early as nine months of age.

While poor growth is well docu­mented in patients with obstructive sleep apnea (2-9), there is controversy

ACKNOWLEDGEMENTS: The authors thank Elinor Rae for typing the manuscript.

REFERENCES I. Parndisc JL. Tonsillectomy and

adenoidectomy. Pediatr C lin North Am 198!;28:881-9 1.

2. Schiffmann R, Fahl:r J , Eidclman A L Obstructive hypertrophic adenoids and tonsils as a cause of infantile fai lure to

rhrive: Reversed hy rons1lleccomy and adcnoidecmmy. Im J Pediatr Otorhinolaryngol 1985;9:38 3-7.

3. G leghorn E. Tonsillar hypertrophy presenting as vomiting and fa ilure to

thrive in todd lers. Published in the proceedings of the North American Society for Pediatric Gastroenccrology and Nutrition, July l 989. (Abst)

4. Lind JG, Lundell BPW. Tonsillar hy-perplasia in children. A cause of obstructive sleep apnea, CO2 retention

488

as to whether recurrent tonsillitis in the absence of obstructive symptoms has an adverse effect on growth (13-15). Grace et al (13) and Mills and Hibben (14) found no significant we ight gain in a group of children post tonsillectomy compared co controls. I lowever, Barr and Osborne ( 15) found a 20% increase in weight in a group of children post tonsillectomy. It would appear that the presence of obstructive symptoms is the principal factor affecting growth ( 13 ).

A review of the literalUre (2-9) sug­gests that with relief of ohstruction, rapid catch -up growth occurs within three to 12 months of surgery. The pres­ent data arc consistent with these re­porrs: case 1 took nine months co achieve Lhe 10th percentile for weight; case 2 regained his previous weight per­centile within two months. Case 2 did nm regain his initia l height percentile within chis period of time, possibly be­cause symptoms recurred and a second operation was needed for relief of ob­struction , and partly because of asthma.

The mechanism of fai lure to thrive in children with obstructive sleep ap­n ea remains speculative. Consistent with previous reports, the fir:;t of the present patients had an inadequate cal­oric intake for age, and demonstrated

and retarded growth. Arch Ocolaryngol 1982; 108:650-4.

5. I lodges S, Wailoo MP. T onsillar enlar-gement and failure co thrive. Br Med J I 987;295:541-2.

6. Kravath RE, Pollak CP, Borlwiccki B. Hypovcntilarion durmg sleep 111

children who have lymphoid airway obstruction treated by nasopharyngcal tube and T and A. Paediatrics I 977;6:865-71.

7. Everett AD, Koch WC, Saulshury FT. Failure to thrive due co ob~trucrive sleep apnea. Clm Ped1atr I 986;26:90-2.

8. Bate TWP, Price DA, Holme CA, McGucken RB. Short stature caused hy obstructive apnea during sleep. Arch Dis C hil<l l 984;59:78-80.

9. Brouillette RT, Fcrnbach SE, Hunt CE. O bstructive sleep apnca in in· fancs and children. J Pediatr 1982; 100: 31-40.

JO. S ills RH. Failure to thrive. The role of clinical and laboratory evaluation>. AmJ D1sCh1ld 1978;132:967-9.

an increase in appetite and weight gain after 1,urgery.

Another theory is that tissue acidosis occurring <luring periods of apnea m;iy impair end organ response to growth fac­tors (8). The reduction of REM sleep in association with obstructive sleep apnea may also impair growth hormone release and further contribute to poor growth. The reversibility of decreased growth hor­mone secretion in a patient with obstruc­tive sleep apnea following tracheoscomy has been demonstrated ( 16).

These two case reports emphasize the importance of considering upper airway obstruction secondary to adeno­tonsillar hypertrophy as a potential cause of fa ilure to thrive in infants. An increased clinical awareness of this en­tity should lead to earlier recognition and surgical intervention in affected children. When one suspects adenoron­sillar hypertrophy as a cause of failure to thrive, one must specifically ask about symptoms a t night, eg, sno ring, laboured breaching, agitated arousal and sleep apnea. Excessive daytime sleepiness b a lso a signific;int clue to the syndrome, reflecting a disturbed sleep pattern. Polygraphic monitoring during sleep can he used to confirm the diag­nosis if there is any doubt.

11. Guillemanault C, Eldridge FL, Simmons FB, cl al. S leep apnca in eighc children. Pediatrics J 976;58:23-30.

12. Yates OW. Adenotonsillar hyper-m1phy and cor pulmonale. Br J Anaesth 1988;61:355-9.

13. Grace A, Veitch D, Ryan R, Barnes N, Coles T. Recurrent tonsillitis and growrh in children. Im J Pediacr Ororhinolaryngol 1988; 16:91-3.

14. Mills RP, Hibbert J. The cffcc~ of recurrent tonsillitis o n growth and cer-vical lymph.:idennpachy in children. Int J Pediatr Otorhinolaryngol 1983;6:77-82.

15. Barr GS, Osborne J. Weight gain in ch ildren following tonsillectomy. J Laryngol Otol 1988; I 02: 595-7.

16. Goldstein SJ, Wu RHK, Thorpy MJ, Shprintzon RS, Marion RE, Saenger P. Reversihility of deficient sleep entramed growth hormone secretion in a boy with achondroplas1a and obstruc-ri ve sleep apnca. Acta Endocrinol 1987;116:95-!0l.

CAN J GASTROENTEROL Vm 4 No 8 NOVEMBER/DECEMBER 1990

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